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02 and P = .04, respectively). Moreover, anaphylaxis was less frequent in patients with profilin sensitization (P = .03). The comparison of patients' data from HRUM with data from HCB showed differences in sensitization to olive tree pollen and profilin (P = .01 and P = .001, respectively). Conclusion This study was undertaken to characterize two large group of subjects from to two regions with differing exposures to pollen. We found that more than 90% of peach-allergic patients in both populations evolved to LTP-Allergy and showed an early onset. Profilin sensitization could be more useful as a severity biomarker than the number of nsLTP, aeroallergen sensitizations or sIgE levels. This could provide clues regarding sensitization and severity patterns that might be relevant in other geographical areas.Background Recent evidence demonstrates that activated eosinophils undergo a distinct form of lytic cell death, accompanied by formation of DNA-based eosinophil extracellular trap (EET) and degranulation, enhancing inflammatory immune responses in asthmatic airways. We previously showed that human blood eosinophils undergo degranulation in response to lysophosphatidylserine (LysoPS), an inflammatory lipid mediator, and strongly express P2Y10, a LysoPS receptor. Methods We evaluated EET, degranulation, and cell death of eosinophils in response to various concentrations of LysoPS. We also compared responsiveness to LysoPS between eosinophils from severe and nonsevere asthmatics. Results Extensive EET formation was elicited from a substantial fraction of stimulated eosinophils in response to 50 μM LysoPS. Analyses for LDH and eosinophil-derived neurotoxin release showed that both lytic cell death and degranulation accompanied EET formation in response to LysoPS. Cytological analyses demonstrated that citrullinated histone 3 was present in the extracellular, filamentous DNA structure embedded with eosinophil granules. The LysoPS-induced EET was independent of ROS production and irrelevant to several signaling pathways examined, but dependent on protein arginine deiminase 4. A low concentration of LysoPS (5 μM) did not induce EET or degranulation, but significantly increased platelet-activating factor-induced degranulation. Eosinophils from severe asthmatics exhibited greater degranulation, but not EET formation, in response to LysoPS (50 μM), than those from nonsevere asthmatics, along with great expression of surface P2Y10. Conclusions We identified a novel function of LysoPS, namely induction of EET in association with cytolysis and degranulation. LysoPS-dependent EET or degranulation plays a potential role in eosinophilic inflammation of severe asthma.Background Acidemia in sick dogs often results from the accumulation of lactic acid. The resulting decrease in blood pH can have many physiologic effects, including alteration of platelet function. Objectives We aimed to evaluate the effect of hyperlactatemia and subsequent acidemia on platelet aggregation in canine blood using impedance aggregometry. Methods Platelet aggregation was measured in blood from 27 healthy dogs using the Multiplate analyzer at baseline and after in vitro addition of two different volumes of lactic acid to adjust the pH. The area under the curve (AUC), reported by the Multiplate analyzer, was used to assess the extent of platelet aggregation in each sample. A linear mixed effects model was used to test for the association between platelet aggregation and pH. The association of baseline platelet aggregation with HCTs, platelet counts, and WBC counts was assessed using Pearson's correlations. Results Acidemia was associated with a significant decrease in platelet aggregation. No significant correlations were detected between platelet aggregation and HCT, platelet count, or WBC count. Platelet aggregation measured using the Multiplate analyzer showed substantial individual variation. Conclusions Worsening acidemia due to the addition of lactic acid caused a mild but significant decrease in platelet aggregation in canine blood. The clinical significance of this change is uncertain but could be important when combined with other abnormalities of hemostasis associated with illness.Cytokines play a key role as mediators in the immuno-pathogenesis of asthma.1 Age at asthma onset and the presence of T-helper 2 mediated eosinophilic airway inflammation have been identified as two important and distinct factors for defining asthma phenotypes,2 but little is known about longitudinal associations between systemic cytokine concentrations and asthma. In a previous investigation of serum cytokine concentrations among 44-year-old adults and asthma phenotypes, we found early-onset persistent asthma (from age 13 to 44 years) was associated with lower levels of interleukin (IL) -10, while asthma remission was associated with lower levels of IL-6 and TNF-α.3 We hypothesised that, in middle-aged people with asthma serum cytokines might predict future asthma persistence beyond 44 years. Published studies regarding these potential associations are largely limited to childhood asthma, with only the Epidemiological study on the Genetics and Environment of Asthma (EGEA study) assessing cytokines profiles and asthma status longitudinally in adults, where they found patients with "high IL-1Ra and high IL-10" serum cytokine profiles had lower risks of worsening asthma control.4.Double-orifice mitral valve (DOMV) is an uncommon congenital anomaly account for 1% of congenital heart disease. selleck inhibitor However, accurate diagnosis and evaluation of valve stenosis or regurgitation and other concomitant congenital anomalies due to DOMV are required to obtain suitable treatment. Two- and three-dimensional echocardiography can contribute valuable functional and anatomic information that can support to reach this goal. Here, we present a case of complete bridge-type DOMV that causes mitral stenosis after surgical repair of the partial atrioventricular septal defect in childhood.Photoautotrophic growth in nature requires the accumulation of energy-containing molecules via photosynthesis during daylight to fuel nighttime catabolism. Many diatoms store photosynthate as the neutral lipid triacylglycerol (TAG). While the pathways of diatom fatty acid and TAG synthesis appear to be well conserved with plants, the pathways of TAG catabolism and downstream fatty acid β-oxidation have not been characterized in diatoms. We identified a putative mitochondria-targeted, bacterial type Acyl-CoA Dehydrogenase (PtMACAD1) that is present in Stramenopile and Hacrobian eukaryotes, but not found in plants, animals or fungi. Gene knockout, protein-YFP tags and physiological assays were used to determine PtMACAD1's role in the diatom Phaeodactylum tricornutum. PtMACAD1 is located in the mitochondria. Absence of PtMACAD1 led to no consumption of TAG at night and slower growth in light/dark cycles compared to wild-type. Accumulation of transcripts encoding peroxisomal-based β-oxidation did not change in response to day/night cycles or to PtMACAD1 knockout.